Specifically, TAL transport defects are associated with hypercalciuria and NaCl wasting, which is absent in the CAII-deficient mice (Figure 3C and Table 1), and deficiencies in the concentrating segments of the distal nephron produce severe phenotypes, which should not respond to water deprivation or ddAVP (Rojek et al., 2006; Kortenoeven et al., 2013). Here, CA2 is linked to Hypercalciuria.